L23: Intro to Psychiatry Flashcards

1
Q

What is a psychiatrist?

A

Physician who specializes in the diagnosis and treatment of mental disorders (MD 4 years, residency 5 years)
Treat patients through: psychotherapy, psychopharmacology, somatic therapies, lifestyle modification

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2
Q

How does the DSM-5 define a mental disorder?

A

A syndrome characterized by clinically significant disturbance in an individuals cognition, emotional regulation, or behaviour that reflects a dysfunction in the psychological, biological, or developmental processes underlying mental function.

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3
Q

What is an important part of the definition of a mental disorder in the DSM-5?

A

Mental disorders are usually associated with significant distress or disability in social, occupational, or other activities
NEED TO BE BOTHERED BY IT
The condition must cause clinically significant distress AND/OR cause difficulties in fxn or disability

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4
Q

What are two examples of things that are not mental disorders?

A
  1. An expectable or culturally approved response to a common stressor or loss
  2. Social deviant behaviour and conflicts that are primarily between the individual and society (unless the deviance results from a dysfunction in the individual)
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5
Q

What are the three different treatments of psychiatric disorders?

A

Psychotherapies: addressing thoughts, behaviours, emotions and relationships through developing insight, changing cognitions and changing behaviours
Pharmacotherapies: drugs that are often symptom specific, not diagnosis specific, drugs names usually reflect intent and not what they actually do (ex antidepressants)
Somatic therapies: involves stimulating neural circuits (ECT, TMS, DBS, Vagal nerve stimulation, phototherapy)

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6
Q

What is the DSM-5 criteria for a Major Depressive Episode (MDE)?

A

At least 5 of below must be present in a 2-week period, and either 1/2 need to be included:
Depressed mood
Diminished interest/pleasure (anhedonia)
Unintentional weight change or change in appetite
Sleep disturbances
Psychomotor agitation
Fatigue/ lethargy/ lack of energy, Guilt/worthlessness
Trouble concentrating or thinking
Recurrent thoughts of death or suicidal ideation

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7
Q

What must the symptoms of MDE do?

A

Be disruptive enough to impair normal fxn
No occur exclusively in the context of schizo or another psych disorder
Not be due to effects of a substance
Occur most days over the two weeks

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8
Q

What is involved in the course of MDD?

A

Average age of onset is 25-30, and may be gradual or sudden onset
MDE is a recurrent illness (after one MDE, the chance of a second is 50%, and after two it is 80%)

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9
Q

Is MDD due more to nature or nurture?

A

MDD is 2-3x more prevalent if there is a first degree relative who suffers from it
Twin/ adoption studies: 20-30% of identical twins are not concordant for MDD
There must be an additional environmental element in addition to genetic vulnerability

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10
Q

What is ACES?

A

Adverse childhood experiences
Negative events that occur in childhood that are associated with increased rate of health conditions
Focus on negative events and does not take into account protective factors
Abuse, neglect, household, familial and environmental exposures
Protective factors may mitigate some of the risk and impact associated with ACES
Higher rates associated with low educational and occupational achievement, higher rates of mental health disorders, substance use, suicide, cancer, diabetes

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11
Q

What are anatomical aspects of MDD?

A

Brain regions most implicated include medial prefrontal cortex, hypothalamus and HPA axis (hypothalamic pituitary adrenal axis), and the hippocampus
Reduced volumes in the brains of individuals with depression likely reflects impaired neurogenesis (due to stress)

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12
Q

What is the lifetime prevalence of MDD? How likely is recovery?

A

In adults: 17%
10-20% for women and 5-10% for men
With increasing severity and chronicity of the initial episode (due in some cases to a delay in receiving effective treatment) the less likely a full recovery is

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13
Q

What is the biogenic amine (monoamine) hypothesis of depression? Why is it flawed?

A

Depression is the result of a functional deficiency of noradrenaline (NA) and/or 5HT (serotonin) at specific synapses in the CNS.
This is an oversimplified definition because depression includes many NT (Glu, AcH, GABA, DA), and neurogenesis, glucocorticoids, inflammation, endocannabinoids, neuroactive steroids

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14
Q

How effective are antidepressants? What causes differences in efficacy between them?

A

Trials show that all antidepressants are more or less equally effective in treatment with 60-80% response rate and 30-40% remission rate
Major differences in antidepressants are due to side effects and metabolism

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15
Q

What is involved in the timeline of antidepressant treatment?

A

Initial treatment for at least one year after remission to reduce rate of relapse
Higher rates of relapse of medication is stopped early
Some individuals end up on longer or continuous treatment if they have repeated ir severe episodes
Increased suicidality after the initiation of an antidepressant may be because patient has increased energy (restless), but mood is low

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16
Q

What is the site of action for MAOIs and Uptake inhibitors?

A

MAOIs work within the presynaptic terminal and uptake inhibitors act on the presynaptic membrane to prevent NT reuptake into the presynaptic terminal

17
Q

What are MAOIs?

A

Inhibit monoamine oxidase and allow amine NT to accumulate within the nerve terminal
It is supposed that this excess NT then flows into the synaptic cleft and onto postsynaptic receptors

18
Q

How to Tricyclic Antidepressants work?

A

They inhibit the reuptake of NA and 5HT into the nerve terminals, resulting in an increased functional availability of these NT amines at central receptors
-triptylines

19
Q

What are SSRIs? What are SNRIs?

A

Selective serotonin reuptake inhibitors, strong inhibitors of 5HT reuptake and , unlike the TCA, they and their metabolites have little effect on NA reuptake into nerve terminals
Serotonin- NA reuptake inhibitors, inhibit the reuptake of both 5HT and Na from synaptic cleft

20
Q

How is ECT used to treat depression?

A

An effective treatment for severe depression (works fast), unknown mode of action, used for treatment resistant depression and depression with psychotic features (hallucinations and delusions)
Can be used on conjunction with antidepressants and antipsychotics, raises mood for 4-6 months and medication is often needed for maintenance
Some ppl receive ongoing ECT for maintenance and prevent relapse

21
Q

What can antidepressants also be used for?

A

Treatment of anxiety, eating and personality disorders, as well as some chronic pain syndromes

22
Q

What is anxiety? What are the four anxiety disorders that we talk about

A

Normal adaptive response to perceived threats of danger
Becomes a disorder when it results in significant impairment in function and personal distress
The 12 month prevalence rate for having an anxiety disorder is around 18%
Panic disorders, social anxiety disorders, specific phobias, GAD

23
Q

What is a panic disorder?

A

Unpredictable and recurrent attacks of panic characterized by upsetting physical symptoms such as tachycardia, chest pain, sweating, tremor, nausea, and overwhelming sensations of fear and loss of control
Often accompanied by compensatory action to help people cope with feelings

24
Q

What is a social anxiety disorder?

A

Extreme and persistent anxiety about social situations, leading to avoidance of those situations or pronounced anxiety attacks on exposure, or anticipation of exposure to the situation

25
Q

What is a specific phobia?

A

Clinically significant anxiety provoked by exposure to a specific feared object or situation, often leading to avoidance behaviour

26
Q

What is Generalized Anxiety Disorder?

A

Excessive anxiety and worry, occurring most days for more than 6 months with symptoms of motor tension, autonomic hyperactivity, apprehensive expectation, vigilance and scanning

27
Q

What is the neurochemical basis of anxiety disorders?

A

Thought to be due to overactivity of neural circuits involved in flight/flight/freeze behaviour
Mostly involve serotonergic and noradrenergic synapses

28
Q

What are anatomical aspects of anxiety?

A

Limbic system involved:
Thalamus: send sights and sounds to specific part of cortex
Amygdala: fear response, signals to LC and hypothalamus and pituitary and activate hormonal response
Hippocampus: stores raw info from senses and emotional tone and links memories to emotional stress
LC: gets signals from amy and sends signals via NA to rest of body to trigger fear response (fight or flight)

29
Q

How are anxiety disorders treated?

A

Combinations of cognitive behavioural therapy (CBT) and medications are often used including antidepressants, benzos, and beta blockers

30
Q

How do benzos work to treat anxiety? Can you become dependent?

A

Benzos interact with binding sites on GABA-A receptor and potentiate GABA-mediated increases in chloride permeability
Psychological dependence does develop (25% of patients), and withdrawal effects occur on cessation of treatment and include anxiety and insomnia (or as severe as seizures and hallucinations)